Hidradenitis suppurativa

"Suppurativa" redirects here. For acrodermatitis continua suppurativa, see Dermatitis repens.

Verneuil’s disease is a chronic inflammatory skin condition primarily affecting areas rich in hair follicles (axillae, groin, anogenital, and inframammary regions). The disease is painful, disabling, and potentially life-threatening due to complications such as septicemia, cardiovascular involvement, surgical complications, and metabolic comorbidities.^[5]

Hidradenitis suppurativa
Other names	Acne inversa, apocrine acne, Verneuil's disease, Velpeau's disease[1]
Hidradenitis suppurativa (Hurley's stage II) in the left armpit
Specialty	Dermatology
Symptoms	Multiple inflamed and swollen skin lesions[2]
Usual onset	Childhood and Young adulthood[2]
Duration	Long-term[2]
Types	Stage I, II, III[1]
Causes	Unknown[3]
Diagnostic method	Based on symptoms[2]
Differential diagnosis	Acne, acne conglobata, pilonidal cysts[2]
Treatment	Warm baths, laser therapy, surgery[2][4]
Medication	Secukinumab, antibiotics, immunosuppressive medication[2]
Frequency	1–4% of people, when mild cases are included[2][3]
Deaths	Rare[1]

Contrary to popular belief, it is not simply a succession of “abscesses,” but rather a chronic inflammation of follicles and associated glands that can cause deep and extensive lesions.^[6]

Prevalence is estimated between 0.5 and 1% of the general population.^[7] Diagnosis is often delayed, with an average lag of 7 years.^[8]

Studies suggest genetic, immunological, and endocrinological involvement (hormonal imbalance, hypercortisolism, metabolic syndrome).^[9]

Management

Management of Verneuil’s disease combines medical, surgical, and supportive approaches.

Medical treatments

• Systemic antibiotics can reduce inflammation but do not induce remission.^[10]
• Biologics, especially anti-TNFα agents (adalimumab), are an option for moderate to severe cases, with partial efficacy in reducing flares.^[11]
• Non-steroidal anti-inflammatory drugs (NSAIDs) are not considered disease-modifying therapy.

Surgery

• The main surgical procedure is wide excision of the diseased area, removing inflamed and scarred tissues.
• This aims to limit local recurrences but may require multiple interventions over a patient’s lifetime.^[12]

Palliative care

• Complete cure of Verneuil’s disease is currently not possible.
• Palliative care should be a key indication in severe and chronic forms, including pain control, psychological support, and social assistance.^[13]
• This approach is essential to improve patients’ quality of life.

Endocrinological assessment

• Several studies suggest involvement of metabolic and hormonal abnormalities, particularly regarding cortisol and insulin resistance.^[14]
• A systematic endocrinological workup is recommended to detect comorbidities (diabetes, metabolic syndrome), frequently associated with severe forms.

Radiotherapy

• In selected refractory cases, low-dose irradiation has been reported to improve resistant lesions, though indications remain limited to highly recurrent cases.^[15]

Low-dose radiotherapy and adalimumab in Verneuil’s disease

Both low-dose radiotherapy and adalimumab (Humira) are therapeutic options studied in Verneuil’s disease (hidradenitis suppurativa, HS), particularly in patients refractory to conventional treatment or ineligible for surgery.

Low-dose radiotherapy

Radiotherapy targets skin lesions, reducing inflammation, follicular proliferation, and fibrosis. It contributes to regression of nodules and superficial fistulas, and reduces pain.

• Efficacy: 78.3% improvement in a German study (2000, n = 231)^[16] ; 72.5% improvement in a Swiss study (2021, n = 40)^[17]

• Side effects: mild skin burns (rare), theoretical long-term risk of carcinogenesis. Overall considered safe at low doses.

Adalimumab (Humira)

Adalimumab is a TNF-α inhibitor approved for moderate to severe HS. It reduces nodules and fistulas.

• Efficacy: about 54% of patients reached HiSCR at week 16 (SOLACE, 2021)^[18] ; 41.8% at week 12 (PIONEER I & II, 2016)^[19]

• Side effects: common mild infections, local injection reactions; rare severe infections and autoimmune disorders. Patient response is variable.

Comparison of treatments

Treatment	Approximate efficacy	Common side effects	Severe adverse events	Overall risk
Low-dose radiotherapy	72–78%	Mild skin burns (rare)	Cutaneous carcinogenesis (theoretical, very rare)	Low
Adalimumab (Humira)	42–54%	Mild infections, local reactions	Severe infections, allergic reactions, autoimmune disorders	Moderate to high

Dermal substitutes and artificial skin in surgical management of Verneuil’s disease

In advanced Verneuil’s disease (hidradenitis suppurativa, HS; Hurley II–III), surgery — particularly wide excision — is often necessary. This approach can leave large skin defects, requiring innovative reconstructive techniques.

Acellular dermal substitutes (Matriderm®)

• A 33-year-old female with refractory HS underwent axillary reconstruction with an acellular dermal substitute (Matriderm®) combined with immediate split-thickness skin grafting. This produced supple, durable skin with good healing, potentially limiting recurrence in the treated area.^[20]

Bilayer dermal regeneration template

• In a study of four patients, a two-step technique was used: wide excision followed by immediate application of a bilayer dermal regeneration template, then closure with a split-thickness graft. No recurrences were observed, though minor complications such as graft or template loss occurred.^[21]

Acellular dermal matrix + split-thickness skin graft as co-graft

• A novel reconstructive method using a co-graft of acellular dermal matrix and split-thickness graft was tested in two cases. It enabled rapid wound closure with good functional and aesthetic outcomes, assessed by laser analysis, cutometry, and quality of life measures.^[22]

Conclusion and perspectives

Acellular dermal substitutes and related techniques offer promising alternatives to conventional secondary healing after excision in severe HS. They may allow for more supple, durable, and aesthetic skin reconstruction, while potentially reducing local recurrences. However, data are limited to very small series; prospective comparative studies are required to confirm these results and define best surgical practices.

Pathophysiology

Verneuil’s disease is a chronic inflammatory disorder of the hair follicle. It begins with follicular obstruction, followed by local inflammation spreading to adjacent tissues, leading to nodules, sinus tracts, and scarring.^[23]

Contrary to earlier belief, it is not a primary infection of sweat glands, but rather a disorder of follicular occlusion (follicular rupture, secondary inflammatory reaction).^[24]

Immunological abnormalities (inappropriate activation of innate and adaptive immunity) and endocrinological factors (possible roles of cortisol and androgens) are also implicated.^[25]

A systematic endocrinological workup (cortisol, androgens, glucose metabolism) is recommended, given the documented links with diabetes and metabolic syndrome.^[26]

Staging and progression

Severity of Verneuil’s disease is classified by the Hurley staging system:

• Stage I: isolated inflammatory lesions, without sinus tracts.
• Stage II: recurrent inflammatory lesions with sinus tracts and scarring, affecting one or more anatomical sites.
• Stage III: diffuse or near-diffuse involvement, with multiple interconnected lesions, extensive sinus tracts, and massive scarring.^[27]

Progression is characterized by alternating active inflammatory phases and partial remissions. The disease is chronic and disabling, with severe forms causing major functional and social limitations.^[28]

Surgical treatment, when indicated, involves complete excision of the affected area to remove inflamed and fibrotic tissues. This is not simple drainage, but wide excision aimed at reducing local recurrences.^[29]

Complications and mortality

Verneuil’s disease leads to numerous physical, psychological, and social complications.

Physical complications

• Formation of scar contractures causing functional limitations.
• Recurrent infections and chronic skin involvement.
• Increased risk of cutaneous squamous cell carcinoma in chronically inflamed areas.^[30]

Pain and mental health

• Severe chronic pain may be resistant to standard treatments and is a major risk factor for depression and suicidal ideation.^[31]
• Several studies report high prevalence of **anxiety and depressive disorders**.

Mortality and hazard ratio

• A Danish cohort study showed HS patients had an all-cause mortality Hazard Ratio of 2.48 compared with the general population.^[32]

Conclusion

• Verneuil’s disease is associated with increased mortality, comparable or superior to certain common cancers.
• These data support recognition of the disease as a potentially life-threatening condition, justifying better multidisciplinary management and systematic access to palliative care.

Comorbidities

Verneuil’s disease is frequently associated with:

• metabolic syndrome and type 2 diabetes;^[33]
• chronic inflammatory bowel diseases (notably Crohn’s disease);^[34]
• increased cardiovascular risk due to systemic inflammation and metabolic comorbidities.^[35]

Psychological and socio-economic impact

Quality of life is severely impaired (DLQI), with high prevalence of depression, anxiety, and suicidal ideation. The disease causes absenteeism, loss of income, and socio-economic vulnerability. Workplace adjustments and social support are essential.^[36][37]

Notes and references

1. "Hidradenitis Suppurativa". NORD (National Organization for Rare Disorders). 2012. Archived from the original on 19 February 2017. Retrieved 26 October 2017.
2. Jemec GB (January 2012). "Clinical practice. Hidradenitis suppurativa". The New England Journal of Medicine. 366 (2): 158–64. doi:10.1056/NEJMcp1014163. PMID 22236226.
3. "Hidradenitis suppurativa". Genetics Home Reference. December 2013. Archived from the original on 5 September 2017. Retrieved 27 October 2017.
4. "Hidradenitis suppurativa". rarediseases.info.nih.gov. 2017. Archived from the original on 28 July 2017. Retrieved 27 October 2017.
5. Thorlacius L, et al. "Increased mortality in patients with hidradenitis suppurativa." Br J Dermatol. 2019.
6. Ingram JR, et al. "Interventions for hidradenitis suppurativa: a Cochrane systematic review." Br J Dermatol. 2016.
7. Revuz JE, et al. "Prevalence and factors associated with hidradenitis suppurativa." J Am Acad Dermatol. 2008.
8. Saunte DM, Jemec GB. "Hidradenitis suppurativa: Advances in diagnosis and treatment." JAMA. 2017.
9. Hotz C, et al. "Endocrine aspects of hidradenitis suppurativa." Dermatoendocrinol. 2016.
10. Ingram JR et al. "Interventions for hidradenitis suppurativa: Cochrane systematic review." Br J Dermatol. 2016.
11. Kimball AB et al. "Two Phase 3 Trials of Adalimumab for Hidradenitis Suppurativa." N Engl J Med. 2016.
12. Jemec GB. "Surgical treatment of hidradenitis suppurativa." Dermatol Clin. 2010.
13. van der Zee HH, Jemec GB. "New insights into the diagnosis, pathogenesis, and treatment of hidradenitis suppurativa." J Am Acad Dermatol. 2015.
14. Kromann CB et al. "Increased prevalence of metabolic syndrome in patients with hidradenitis suppurativa." J Am Acad Dermatol. 2014.
15. Matusiak Ł, et al. Radiotherapy as a treatment option in hidradenitis suppurativa. J Eur Acad Dermatol Venereol. 2018.
16. Schneider HW (2000). "Radiotherapy of hidradenitis suppurativa – still valid today". Strahlentherapie und Onkologie.
17. Zimmermann F (2021). "Low-dose radiotherapy in hidradenitis suppurativa: a retrospective study". Dermatology (Basel, Switzerland). 237 (3): 357–364. doi:10.1159/000514027. PMID 33535201.
18. Lee J (2021). "Efficacy of adalimumab in hidradenitis suppurativa: SOLACE study". Journal of the European Academy of Dermatology and Venereology. 30 (6): 989–994. doi:10.1111/jdv.13216. PMC 5034809. PMID 26201313.
19. Kimball J (2016). "Adalimumab for hidradenitis suppurativa: PIONEER I and II trials". New England Journal of Medicine. doi:10.1056/NEJMoa1504370.
20. Dhannoon A (2021). "Acellular dermal substitute use in the reconstruction of axillary hidradenitis suppurativa". JPRAS Open. 31: 129–133. doi:10.1016/j.jpra.2021.11.003. PMC 8777236. PMID 35079618.
21. Manfredini M (2020). "Novel surgical approach for axillary hidradenitis suppurativa using a bilayer dermal regeneration template: a retrospective case study". Skin Appendage Disorders. 6 (4): 195–201. doi:10.1159/000507297. PMC 7445542. PMID 32903939.
22. Gierek M (2023). "Co-Graft of Acellular Dermal Matrix and Split Thickness Skin Graft—A New Reconstructive Surgical Method in the Treatment of Hidradenitis Suppurativa". Journal of Clinical Medicine. 12 (6): 2112. doi:10.3390/jcm12062112. PMC 10056202. PMID 36983115.
23. Jemec GB. "Clinical practice. Hidradenitis suppurativa." N Engl J Med. 2012.
24. Revuz JE. "Hidradenitis suppurativa." J Eur Acad Dermatol Venereol. 2009.
25. Hotz C, et al. "Endocrine aspects of hidradenitis suppurativa." Dermatoendocrinol. 2016.
26. Sabater J, et al. "Metabolic syndrome in hidradenitis suppurativa." J Eur Acad Dermatol Venereol. 2017.
27. Hurley HJ. "Axillary Hidradenitis: A Clinical, Pathological and Surgical Study." In: Roenigk & Roenigk’s Dermatologic Surgery. 1989.
28. Revuz JE. "Hidradenitis suppurativa: epidemiology, clinical features, and treatment." Ann Dermatol Venereol. 2011.
29. Jemec GB. "Surgical treatment of hidradenitis suppurativa." Dermatol Clin. 2010.
30. Lapins J et al. "Squamous cell carcinoma complicating hidradenitis suppurativa: a report of 6 cases." Arch Dermatol. 2001.
31. van der Zee HH et al. "Quality of life and depression in hidradenitis suppurativa patients." Br J Dermatol. 2010.
32. Kromann CB et al. "Increased risk of death in patients with hidradenitis suppurativa." Br J Dermatol. 2017.
33. Shalom G, et al. Hidradenitis suppurativa and comorbidities: a systematic review. J Am Acad Dermatol. 2020.
34. Garg A, et al. Comorbidity profiles of patients with hidradenitis suppurativa. JAMA Dermatol. 2018.
35. Sabat R, et al. Hidradenitis suppurativa. Nat Rev Dis Primers. 2020.
36. Burden of Hidradenitis Suppurativa: A Systematic Literature Review. Dermatol Ther (Heidelb). 2024.
37. Schneider-Burrus S, et al. The impact of hidradenitis suppurativa on professional life. Br J Dermatol. 2023.

External links

• [http://www.afrh.org AFRH – French Association for Research on Hidradenitis

Terminology

Although hidradenitis suppurativa is often called acne inversa, it is not a form of acne. Hidradenitis suppurativa lacks the core defining features of acne, such as the presence of closed comedones and increased sebum production.^[1]

Causes

The exact cause of hidradenitis suppurativa remains unknown,^[2][4] and there has, in the recent past, been notable disagreement among experts in this regard.^[5] The condition, however, likely stems from both genetic and environmental causes.^[3] Specifically, an immune-mediated pathology has been proposed,^[2] although environmental factors have not been ruled out.^[3]

Lesions will occur in any body area with hair follicles,^[5] and/or sweat glands.^[6] Areas such as the axilla, groin, and perineal region are more commonly involved. This theory includes most of these potential indicators:^[7]

• Post-pubescent individuals^[8]
• Blocked hair follicles or blocked apocrine sweat glands
• Excessive sweating
• Androgen dysfunction
• Genetic disorders that alter cell structure

The historical understanding of the disease suggests dysfunctional apocrine glands^[9] or dysfunctional hair follicles,^[10] possibly triggered by a blocked gland, which creates inflammation, pain, and a swollen lesion.

Triggering factors

Several triggering factors should be taken into consideration:

• Obesity^[11] is an exacerbating rather than a triggering factor,^[12] through mechanical irritation, occlusion, and skin maceration.
• Tight clothing,^[11] and clothing made of heavy, nonbreathable materials^[13]
• Deodorants, depilation products, shaving of the affected area – their association with HS is still an ongoing debate among researchers.^[14]
• Drugs, in particular oral contraceptive pills,^[15] cigarette smoking,^[16][17] and lithium.^[18]
• Hot and especially humid climates.^[19]
• Stress^[17]

Predisposing factors

• Genetic factors:^[12] an autosomal dominant inheritance pattern has been proposed.^[20]
• Endocrine factors:
  • Sex hormones, especially an excess of androgens, are thought to be involved, although the apocrine glands are not sensitive to these hormones.^[21] Women often have outbreaks before their menstrual period and after pregnancy; HS severity usually decreases during pregnancy and after menopause.
  • Diabetes mellitus is common in hidradenitis suppurativa and seems to be a risk factor.^[22]

Some cases have been found to result from mutations in the NCSTN, PSEN1, or PSENEN genes. The genes produce proteins that are all components of a complex called gamma- (γ-) secretase. This complex cuts apart (cleaves) many different proteins, which is a crucial step in several chemical signaling pathways. One of these pathways, known as notch signaling, is essential for the normal maturation and division of hair follicle cells and other types of skin cells. Notch signaling influences normal immune system function. Studies suggest mutations in the NCSTN, PSEN1, or PSENEN genes impair notch signaling in hair follicles. Although little is known about the mechanism, abnormal notch signaling appears to promote the development of nodules and lead to skin inflammation.^[23] In addition, the composition of the intestinal microflora and as a consequence dietary patterns appear to play a role. Although dysbiosis of the cutaneous microbiome apparent in HS is not observed, the concurrent existence of inflammatory gut and skin diseases has led to the hypothesis of a gut-skin axis in which gut microbiota is implicated. Indeed, analysis of bacterial taxa in fecal samples from HS patients supports the possibility of a role for intestinal microbial alterations in this chronic inflammatory skin disease.^[24]

Precocious puberty is more common among children and adolescents with hidradenitis suppurativa (HS) compared to those without the condition, according to a recent case-control study.^[25]

An analysis of the Explorys database revealed that pediatric patients with precocious puberty have double the risk of developing HS, even after adjusting for factors like demographic characteristics and body mass index (BMI).^[26]

Diagnosis

Early diagnosis is essential in avoiding tissue damage. However, HS is often misdiagnosed or diagnosed late due to healthcare professionals not being aware of the condition or people not consulting with a physician.^[27][28] Globally, the diagnosis is delayed more than 7 years in average after symptoms appear. This is much longer than with other skin conditions.^[29]

Stages

 

Hidradenitis suppurativa stage III on abdomen: Skin is red and inflamed, constantly draining a malodorous blood/pus mixture. Pain is severe.

 

Hidradenitis suppurativa. This lesion is about 4 inches across.

 

Micrograph of hidradenitis suppurativa: Sinus tracts [(A), arrow], active inflammation, and rupture [(B), asterisks] of the follicular epithelium with “floating” hair fragments (B), arrowSubsequently, a secondary inflammatory response is induced with an influx of numerous neutrophils [(C), arrows] and granulomatous foreign body reaction with giant cells [(C), asterisks].^[30]

Hidradenitis suppurativa presents itself in three stages.^[9][31] Due to the large spectrum of clinical severity and the severe impact on quality of life, a reliable method for evaluating HS severity is needed.^{[citation needed]}

Hurley's staging system

Hurley's staging system was the first classification system proposed and is still in use for the classification of patients with skin diseases (i.e., psoriasis, HS, acne). Hurley separated patients into three groups based largely on the presence and extent of cicatrization and sinuses. It has been used as a basis for clinical trials in the past and to determine appropriate therapy for patients. These three stages are based on Hurley's staging system, which relies on the subjective extent of the diseased tissue. Hurley's three stages of hidradenitis suppurativa are:^[32]

Stage	Characteristics
I	Solitary or multiple isolated abscess formation without scarring or sinus tracts (A few minor sites with rare inflammation; may be mistaken for acne.)
II	Recurrent abscesses, single or multiple widely separated lesions, with sinus tract formation (Frequent inflammation restricts movement and may require minor surgery such as incision and drainage.)
III	Diffuse or broad involvement across a regional area with multiple interconnected sinus tracts and abscesses (Inflammation of sites to the size of golf balls, or sometimes baseballs; scarring develops, including subcutaneous tracts of infection – see fistula. Obviously, patients at this stage may be unable to function.)

Sartorius staging system

The Sartorius staging system is more sophisticated than Hurley's. Sartorius et al. suggested that the Hurley system is not sophisticated enough to assess treatment effects in clinical trials during research. This classification allows for better dynamic monitoring of the disease severity in individual patients. The elements of this staging system are:^[33]

• Anatomic regions involved (axilla, groin, gluteal, or other region or inframammary region left or right)
• Number and types of lesions involved (abscesses, nodules, fistulas or sinuses, scars, points for lesions of all regions involved)
• The distance between lesions, in particular, the longest distance between two relevant lesions (i.e., nodules and fistulas in each region or size if only one lesion is present)
• The presence of normal skin in between lesions (i.e., if all lesions are separated by normal skin)

Points are accumulated in the above categories and added to give a regional and total score. In addition, the authors recommend adding a visual analog scale for pain or using the dermatology life quality index (DLQI, or the 'skindex') when assessing HS.^[34]

Treatment

Treatment depends upon the presentation and severity of the disease. Due to the poorly studied nature of the disease, the effectiveness of medications and therapies was unclear.^[35] Clear and sensitive communication from health care professionals, and social and psychological interventions can help manage the emotional impact of the condition and aid necessary lifestyle changes.^[27][28] In May 2023, the European Commission (EC) approved Cosentyx (secukinumab) for active moderate to severe hidradenitis suppurativa in adults.^[36]

Other possible treatments include the following:

Cryotherapy

Cryotherapy has demonstrated efficacy against the disease, with 88% of persistent lesions resolving in a clinical trial of 23 patients.^[37]

Lifestyle

Warm baths may be tried in those with mild disease.^[38] Weight loss and smoking cessation are recommended.^[39]

Medication

• Antibiotics: taken by mouth, these are used for their anti-inflammatory properties rather than to treat infection. Most effective is a combination of rifampicin and clindamycin given concurrently for 2–3 months. Popular antibiotics also include tetracycline and minocycline.^[40] Topical clindamycin has been shown to have an effect in double-blind placebo-controlled studies.^[41] In a retrospective review and telephone survey, intravenous ertapenem therapy showed clinical improvement with 80.3% of subjects reporting medium to high satisfaction and 90.8% would recommend ertapenem to other patients.^[42]
• Corticosteroid injections, also known as intralesional steroids, can be useful for localized disease if the drug can be prevented from escaping via the sinuses.
• Antiandrogen therapy, hormonal therapy with antiandrogenic medications such as spironolactone, flutamide, cyproterone acetate, ethinylestradiol, finasteride, dutasteride, and metformin, are effective in clinical studies.^[43][44][45] However, the quality of available evidence is low and does not presently allow for robust evidence-based recommendations.^[43][44]
• Intravenous infusion or subcutaneous injection of anti-inflammatory (TNF inhibitors; anti-TNF-alpha) drugs such as infliximab, and etanercept^[46] This use of these drugs is not currently approved in the United States by the Food and Drug Administration (FDA) and is somewhat controversial.^{[citation needed]}
• Biologics: Various biologics can improve HS lesions.^[47] Specifically adalimumab at weekly intervals is useful.^[48] Adalimumab and secukinumab^[49][50] are both approved by the FDA for the treatment of HS as of 2023.
• Topical isotretinoin is usually ineffective in people with HS, and is more commonly known as a medication for the treatment of acne vulgaris. Individuals affected by HS who responded to isotretinoin treatment tended to have milder cases of the condition.^[51]
• Zinc and nicotinamide, at doses of 90 mg and 30 mg respectively, have shown efficacy against mild to moderate hidradenitis suppurativa in a controlled retrospective clinical trial.^[52]

Surgery

When the process becomes chronic, wide surgical excision is the procedure of choice.

Wounds in the affected area do not heal by secondary intention, and immediate or delayed application of a split-thickness skin graft is an option.^[7] Another option is covering the defect with a perforator flap. With this technique, the (mostly totally excised) defect is covered with tissue from an area nearby. For example, the axilla with a fully excised defect of 15 × 7 cm can be covered with a thoracodorsal artery perforator flap.^{[citation needed]}. A less invasive excision procedure called Skin-Tissue-sparing Excision with Electrosurgical Peeling or "STEEP" has also been developed for treating moderate to severe disease.^[53]

Laser hair removal

Further information: Laser ablation § Medicine

The 1064 nm wavelength (near-infrared) laser for hair removal may aid in the treatment of HS.^[54] A randomized control study has shown improvement in HS lesions with the use of a Nd:YAG laser.^[55]

Botox injection

A 2022 study reported that administration of Botulinum toxin resulted in either clinical improvement or improved quality of life in 96.8% (n = 30/31) of HS patients. The level of evidence was moderate. It concluded that the treatment was a safe and potentially effective alternative for hidradenitis suppurativa patients resistant to standard-of-care therapies.^[56]

Prognosis

 

Hidradenitis suppurativa stage III. Open lesions are extremely painful.

 

Hidradenitis suppurativa stage III. Inflamed lesion.

In stage III disease, as classified by Hurley's staging system, fistulae left undiscovered, undiagnosed, or untreated can rarely lead to the development of squamous cell carcinoma in the anus or other affected areas.^[57][58] Other stage III chronic sequelae may also include anemia, multi-localized infections, amyloidosis, and arthropathy. Stage III complications have been known to lead to sepsis, but clinical data are still uncertain.

Comorbidities and complications

Endocrine diseases are more common in people who have HS.^[59] Diabetes mellitus may be both a causal factor contributing to the evolution and/or severity of HS and a consequence of inflammation in HS.^[22][60] Thyroid disorders are also more common in patients with HS.^[61]

• Contractures and reduced mobility of the lower limbs and axillae due to fibrosis and scarring occur. Severe lymphedema may develop in the lower limbs.
• Local and systemic infections (meningitis, bronchitis, pneumonia, etc.), are seen, which may even progress to sepsis.
• Higher risk for diabetes mellitus, high blood pressure, heart attacks, and metabolic syndrome.^[22] Persons affected by HS have reduced insulin sensitivity (SPINA-GR), which, if uncompensated by increased pancreatic beta cell function, can result in prediabetes and overt diabetes mellitus.^[62] Treatment of HS may contribute to remission of diabetes.^[60]
• HS is associated with an increased risk of polycystic ovarian syndrome.^[63][64]
• Interstitial keratitis
• Pyoderma gangrenosum^[64]
• Pilonidal disease^[64]
• Dyslipidemia^[64]
• Anal, rectal, or urethral fistulae^{[65][ISBN missing]}
• Normochromic or hypochromic anemia^[66]
• People with HS may be at increased risk for autoimmune disorders, including ankylosing spondylitis, rheumatoid arthritis, psoriatic arthritis, and inflammatory bowel diseases, such as Crohn's disease.^[64][67]
• Squamous cell carcinoma has been found on rare occasions in chronic hidradenitis suppurativa of the anogenital region.^[68] The mean time to the onset of this type of lesion is 10 years or more and the tumors are usually highly aggressive.
• Tumors of the lung and oral cavity, and liver cancer^[69]
• Hypoproteinemia and amyloidosis, which can lead to kidney failure and death^[70]
• Seronegative and usually asymmetric arthropathy: pauciarticular arthritis, polyarthritis/polyarthralgia syndrome.^[71]

Impact on mental health

HS is a painful and socially isolating condition that leads to a negative impact on mental health as well. A 2020 meta-analysis found that 21% of people with HS have depression, including major depression and 12% have anxiety, including generalized anxiety disorder and a higher risk of suicide.^[64][72] A 2020 study found that people with HS have suicide rates more than double the rates in controls, and also have a higher risk of attempting suicide.^[73]

Epidemiology

Prevalence

Estimates of the prevalence of HS vary worldwide, and there is no accepted generalization. In the US, the prevalence is estimated to be 0.1% while in Europe it is thought to be 1% or more.^[73]

Sex

In North America and Europe, women are three times more likely to have HS. However, in South Korea, men are twice as likely to have HS.^[73]

Age

HS is the most prevalent in people in their 40s and 50s.^[73]

History

• From 1833 to 1839, in a series of three publications, Velpeau identified and described a disease now known as hidradenitis suppurativa.^[74]
• In 1854, Aristide Verneuil described hidradenitis suppurativa as hidrosadénite phlegmoneuse ("phlegmonous hidrosadenitis"). This is how HS obtained the name "Verneuil's disease".^[75]
• In 1922, Paul Schiefferdecker hypothesized a pathogenic link between "acne inversa" and human sweat glands.^[76]
• In 1956, Pillsbury et al.^[77] coined the term follicular occlusion triad for the common association of hidradenitis suppurativa, acne conglobata and dissecting cellulitis of the scalp. Modern clinical research still employs Pillsbury's terminology for these conditions' descriptions.^[78]
• In 1975, Plewig and Kligman, following Pillsbury's research path, modified the "acne triad", replacing it with the "acne tetrad: acne triad, plus pilonidal sinus".^[79] Plewig and Kligman's research follows in Pillsbury's footsteps, offering explanations of the symptoms associated with hidradenitis suppurativa.
• In 1989, Plewig and Steger's research led them to rename hidradenitis suppurativa, calling it "acne inversa" – which is not still used today in medical terminology, although some individuals still use this outdated term.^[80]

A surgeon from Paris, Velpeau, described an unusual inflammatory process with the formation of superficial axillary, submammary, and perianal abscesses, in a series of three publications from 1833 to 1839. One of his colleagues, also located in Paris, named Verneuil, coined the term hidrosadénite phlegmoneuse about 15 years later. This name for the disease reflects the former pathogenetic model of acne inversa, which considered inflammation of sweat glands as the primary cause of hidradenitis suppurativa. In 1922, Paul Schiefferdecker suspected a pathogenic association between acne inversa and apocrine sweat glands. In 1956, Pillsbury postulated follicular occlusion as the cause of acne inversa, which they grouped together with acne conglobata and perifolliculitis capitis abscendens et suffodiens ("dissecting cellulitis of the scalp") as the "acne triad". Plewig and Kligman added another element to their acne triad, pilonidal sinus. Plewig et al. noted that this new "acne tetrad" includes all the elements found in the original "acne triad", in addition to a fourth element, pilonidal sinus. In 1989, Plewig and Steger introduced the term "acne inversa", indicating a follicular source of the disease and replacing older terms such as "Verneuil disease".

Author	Year	Findings
Velpeau	1839	First description of hidradenitis suppurativa
Verneuil	1854	"Hidrosadénite phlegmoneuse"
Pillsbury	1956	Acne triad (hidradenitis suppurativa, perifolliculitis capitis abscendens et suffodiens, acne congoblata)
Plewig & Kligman	1975	Acne tetrad (acne triad + pilonidal sinus)
Plewig & Steger	1989	Acne inversa

Other names

Hidradenitis suppurativa has been referred to by multiple names in the literature and various cultures. Some of these are also used to describe different diseases or specific instances of this disease.^[31]

• Acne conglobata – not really a synonym – this is a similar process but in classic acne areas of the chest and back
• Acne inversa – a proposed new term^[81][82] which has not gained widespread favor.^[83]
• Apocrine acne – an outdated term based on the disproven^{[citation needed]} concept that apocrine glands are primarily involved, though many do have apocrine gland infection
• Apocrinitis – another outdated term based on the same thesis
• Fox-den disease – a term not used in medical literature, based on the deep fox den–like sinuses
• Hidradenitis supportiva – a misspelling
• Pyodermia fistulans significa – now considered archaic
• Verneuil's disease – recognizing the surgeon whose name is most often associated with the disorder as a result of his 1854–1865 studies^[84]

Histology

Author	Year	Major features
Plewig & Steger[80]	1989	Initial hyperkeratosis of the follicular infundibulum. Bacterial super-infection and follicle rupture. Granulomatous inflammatory reaction of the connective tissue. Apocrine and eccrine sweat glands secondarily involved.
Yu & Cook[85]	1990	Cysts and sinus tracts lined with epithelium, in part with hair shafts. Inflammation of apocrine sweat glands only if eccrine sweat glands and hair follicles are also inflamed.
Boer & Weltevreden[86]	1996	Primary inflammation of the follicular infundibulum. Apocrine sweat glands are secondarily involved.

Society and culture

Experiences of people with HS

HS can have a strong negative impact on people's lives, as well as physical and mental health. People with HS often feel stigmatized and embarrassed by their condition. Many try to hide the symptoms, which can lead to impaired relationships and social isolation. A multidisciplinary approach by healthcare professionals, social support networks, and psychological interventions can contribute to a better quality of life.^[27][28] Compared to other skin diseases, HS has one of the highest Dermatology Life Quality Index (DLQI) scores.^[87]

References

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External links

• Hidradenitis suppurativa at American Academy of Dermatology Association
• Hidradenitis suppurativa at British Association of Dermatologists
• Hidradenitis Suppurativa Foundation